Evidence map›Paper›PMID 24312908›Full record

ArticleBioMed research international2013

Indomethacin-enhanced anticancer effect of arsenic trioxide in A549 cell line: involvement of apoptosis and phospho-ERK and p38 MAPK pathways.

Ali Mandegary, Maryam Torshabi, Mohammad Seyedabadi, Bagher Amirheidari, Elham Sharif, Mohammad Hossein Ghahremani

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  4. Review
  5. Review
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  7. A candidate for lung cancer treatment: arsenic trioxide.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    Review
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  13. Simvastatin downregulates expression of TGF-βRII and inhibits proliferation of A549 cells via ERK.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Ali MandegaryNeuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman 7619813159, Iran.
Maryam Torshabi
Mohammad Seyedabadi
Bagher Amirheidari
Elham Sharif
Mohammad Hossein Ghahremani
Kerman University of Medical Sciences · IRBushehr University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFocusing on novel drug combinations that target different pathways especially apoptosis and MAPK could be a rationale for combination therapy in successful treatment of lung cancer. Concurrent use of cyclooxygenase (COX) inhibitors with arsenic trioxide (ATO) might be a possible treatment option.

methodsCytotoxicity of ATO, dexamethasone (Dex), celecoxib (Cel), and Indomethacin (Indo) individually or in combination was determined at 24, 48, and 72 hrs in A549 lung cancer cells. The COX-2 gene and protein expression, MAPK pathway proteins, and caspase-3 activity were studied for the most cytotoxic combinations.

resultsThe IC50s of ATO and Indo were 68.7 μmol/L and 396.5 μmol/L, respectively. Treatment of cells with combinations of clinically relevant concentrations of ATO and Indo resulted in greater growth inhibition and apoptosis induction than did either agent alone. Caspase-3 activity was considerably high in the presence of ATO and Indo but showed no difference in single or combination use. Phosphorylation of p38 and ERK1/2 was remarkable in the concurrent presence of both drugs.

conclusionsCombination therapy with ATO and Indo exerted a very potent in vitro cytotoxic effect against A549 lung cancer cells. Activation of ERK and p38 pathways might be the mechanism of higher cytotoxic effect of ATO-Indo combination.

Indexed as

Antineoplastic AgentsApoptosisArsenicalsArsenic Trioxidebcl-2-Associated X ProteinCaspase 3CelecoxibCell ProliferationCyclooxygenase 2DexamethasoneDose-Response Relationship, DrugDrug SynergismEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHumansAntineoplastic AgentsArsenicalsArsenic Trioxidebcl-2-Associated X ProteinCaspase 3CelecoxibCyclooxygenase 2DexamethasoneExtracellular Signal-Regulated MAP KinasesIndomethacinOxidesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktPTGS2 protein, humanPyrazolesRNA, MessengerSulfonamides

Identifiers

PMID24312908
PMCPMC3842073
OpenAlexW2106075350

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.